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Daniel T. Starczynowski

Researcher at Cincinnati Children's Hospital Medical Center

Publications -  110
Citations -  9209

Daniel T. Starczynowski is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Myeloid & Myeloid leukemia. The author has an hindex of 31, co-authored 87 publications receiving 7958 citations. Previous affiliations of Daniel T. Starczynowski include BC Cancer Research Centre & Boston University.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Identification of miR-145 and miR-146a as mediators of the 5q– syndrome phenotype

Daniel T. Starczynowski, +13 more
- 01 Jan 2010 - 
TL;DR: Deletes chromosome 5q and identifies Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs.
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Deregulation of innate immune and inflammatory signaling in myelodysplastic syndromes.

Irene Ganan-Gomez, +9 more
- 12 Mar 2015 - 
TL;DR: There is compelling evidence that the deregulation of innate immune and inflammatory signaling also affects other cells from the immune system and the BM microenvironment, which establish aberrant associations with hematopoietic precursors and contribute to the MDS phenotype, which should be considered as one of the driving forces in the pathogenesis of MDS.
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Targeting IRAK1 as a Therapeutic Approach for Myelodysplastic Syndrome

Garrett W. Rhyasen, +20 more
- 08 Jul 2013 - 
TL;DR: It is identified that IRAK1, an immune-modulating kinase, is overexpressed and hyperactivated in MDSs and this finding implicate IRAK 1 as a drugable target in M DSs.
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TRAF6 is an amplified oncogene bridging the RAS and NF-κB pathways in human lung cancer

Daniel T. Starczynowski, +10 more
- 03 Oct 2011 - 
TL;DR: The findings show that TRAF6 is an oncogene that is important for RAS-mediated oncogenesis and provide a mechanistic explanation for the previously apparent importance of constitutive NF-κB activation in RAS -driven lung cancers.